Interpretive Summary: A review chapter on aphid transmission of Citrus tristeza virus is provided for a book on “Vector-Mediated Transmission of Plant Pathogens”. Early long-distance movement of citrus was by seed and, since tristeza virus is not seed-transmitted, citrus remained tristeza-free in new locations. Transcontinental shipment via ships from the early 19th century permitted transport of tristeza-infected trees or cuttings to new regions. From these plantings, tristeza virus was spread by aphid vectors and by graft propagation. Following this, epidemics of tristeza on sour orange rootstock occurred in many new regions. The rapid death of citrus on sour orange rootstocks caused by a virus-induced incompatibility at the budunion. Four major aphid species transmit tristeza virus: Toxoptera citricida, T. aurantii, Aphis gossypii and A. spiraecola. The host range of T. citricida is restricted to citrus and citrus relatives; whereas the other three aphids have a wide host range outside of the citrus family. This is significant because the host range of tristeza is restricted to citrus and citrus relatives. Tristeza virus transmission by aphids is semi-persistent since the virus is foregut-borne in the vector and the virus is phloem-limited in citrus. Vector transmission occurs when aphids feeds in phloem-sieve elements so virus acquisition inoculation time generally is optimal at approximately 24-h. The aphid transmits the virus as soon as it acquires the pathogen (no latent period) and immature aphids cannot transmit after a molt unless the virus is reacquired. Populations of tristeza in an infected tree are comprised of genetic variants due to viral mutations and recombination in different citrus host cultivars. Aphid transmission separates these viral variants and, thus, has a profound influence on which strains are spread and what diseases are induced. Some virus strains are virulent and cause stem pitting in sweet orange and grapefruit while others are mild and symptomless on tolerant citrus-rootstock combinations. The determinants of aphid transmission are unknown but coat protein-mediated transmission and viral encoded helper components are discussed to provide information on possible mechanisms of transmission based on other virus-vector models. Current research focuses on examining the role of viral or host proteins in tristeza transmission. With knowledge of a number of fully sequenced tristeza virus strains and full-length infectious cDNA clones, it is now possible to determine gene function in aphid transmission.

Technical Abstract:
A review chapter on aphid transmission of Citrus tristeza virus is provided for a book on “Vector-Mediated Transmission of Plant Pathogens”. Earliest uses of citrus goes back over two millennia as items of trade, gifts and medicinal compounds. Citrus propagation during this period was by seed and since tristeza virus is not seed transmissible, citrus planting in new areas were tristeza-free. With the onset of transcontinental shipping by ocean-faring ships from the early 19th century, transport of tristeza-infected trees or cuttings to new regions occurred. From these plantings, tristeza virus was spread by aphid vectors and by graft propagation. Subsequently, epidemics of tristeza on sour orange rootstock occurred in many new regions. The rapid death of citrus on sour orange rootstock caused by a virus-induced incompatibility at the budunion. Four major aphid species transmits tristeza virus: Toxoptera citricida, T. aurantii, Aphis gossypii and A. spiraecola. The host range of T. citricida is restricted to citrus and citrus relatives; whereas the other three aphids have a wide host range outside of the citrus family. This has epidemiological significance because the host range of tristeza is restricted to citrus and citrus relatives. Tristeza virus transmission by aphids is semi-persistent since the virus is foregut-borne in the vector and the virus is phloem-limited in citrus. The aphid transmits the virus as soon as it acquires the pathogen (no latent period) and but aphid instars cannot transmit after a molt unless it reacquires the virus. The most efficient vector for tristeza virus is T. citricida and tristeza problems are most severe when it is present. A. gossypii is not as efficient as T. citricida but, nevertheless, can transmit some strains efficiently. A. spiraecola and T. aurantii are inefficient vectors and reasons for vector specificity is unknown. Vector transmission of tristeza virus is semi-persistent and the virus is foregut-borne in the vector and phloem-limited in its citrus host where replication occur. Vector transmission occurs when aphids feeds in phloem-sieve elements so virus acquisition inoculation time generally is optimum at approximately 24-h each. This correlates to the amount of time needed by aphids to penetrate and feed (involving salivation, ingestion-egestion) in phloem. Widespread tristeza dissemination takes only 2-4 year by T. citricida; while tristeza spread by the other aphids takes from 8-15 years or longer and result in a different spatial pattern of infected trees in the field. Populations of tristeza in an infected tree are comprised of genetic variants due to viral mutations and recombinations that occur in infected trees among different host cultivars. Aphid transmission separates these viral variants and, thus, has a profound influence on what strains are spread and what diseases are induced. Some virus strains are virulent and cause stem pitting in sweet orange and grapefruit while others are mild and symptomless on tolerant citrus-rootstock combinations. Determinants of aphid transmission is unknown but coat protein-mediated transmission and viral encoded helper components is discussed to provide information on several speculative modes based on other virus-vector models. Current research focuses on the role of viral or host proteins in tristeza transmission. With knowledge of a number full-length tristeza virus genomes of various strains and full-length cDNA clones, it is now possible develop constructs of individual genes which can be mutated to determine function in aphid transmission.